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Anesthesia-phar > Adrenergic Agonist Medications > Flashcards

Adrenergic Agonist Medications Flashcards

1
Q

List drugs in the Sympathomimetic Amines class

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
  • Isoproterenol
  • Dobutamine
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2
Q

Direct Acting Alpha Agonists

A

Phenylephrine

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3
Q

Other Inotropes

A
  • Vasopressin
  • Milrinone
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4
Q

Mixed Function Agonists

A

•Ephedrine

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5
Q

Alpha 2 Agonists

A

•Clonidine

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6
Q

Beta 2 Agonists

A

•Albuterol

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7
Q

Class of Epinephrine & Route

A

Class: Endogenous catecholamine, adrenergic agonist

Route: IV, IM, Inhalational

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8
Q

Mechanism of Action of Epinephrine

A

Agonizes B1, B2 , A1 and A2 receptors, triggering a G protein response to increased cAMP which increases Ca, resulting in increase BP, CO , bronchial relaxation, & stabilization of mast cells

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9
Q

Clinical Use and Dosing of Epinephrine

A

Cardiac arrest, shock: 1 mg

Anaphylaxis: 100-500 mcg

Infusion: 2 – 20 mcg/min

  • Low dose infusion – beta agonism predominates
  • Medium dose infusion – equal beta and alpha agonism
  • High dose infusions – alpha agonism predominates

Mixed with local anesthetics to decrease systemic absorption 1:200,000 (5mcg/mL of epinephrine)

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10
Q

Onset and DOA of Epinephrine

A

Onset: 1 minute

Duration: 5 – 10 minutes

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11
Q

Metabolism and Excretion of Epinephrine

A

Metabolism: MAO, COMT

Elimination: Renally excreted

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12
Q

Epinephrine may cause ___

A

tachycardia, arrythmias, angina, hypertension, decrease perfusion to splanchnic organs and uterus, and gangrene in digits

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13
Q

Avoid adding epinephrine to ____.

A

peripheral nerve blocks

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14
Q

Caution the use of Epinephrine in patients with ____

A

CAD, hyperthyroidism and pheochromocytoma

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15
Q

Class of Norepinephrine

A

Endogenous catecholamine, adrenergic agonist

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16
Q

Mechanism of Action of Norepinephrine

A

•Agonizes A1, A2 and weakly B1 receptors, triggering a G protein response to increase cAMP which increases Ca, resulting in increased BP and decreased perfusion to splanchnic organs

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17
Q

Clinical Use and Absorption of Norepinephrine

A

Clinical Use: First-line vasopressor for septic shock

Absorption: IV

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18
Q

Dosing, Onset and DOA of Norepinephrine

A

Infusion: 1 – 20 mcg/min

Onset: 1 minute

DOA: 2 – 10 minutes

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19
Q

Metabolism and Excretion of Norepinephrine

A

Metabolism: MAO, COMT

Elimination: Renally excreted

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20
Q

Norepinephrine may cause ____.

A

bradycardia (baroreceptor reflex), hypertension, profound decrease perfusion to splanchnic organs and uterus

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21
Q

Avoid adding norepinephrine to ___.

A

peripheral nerve blocks

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22
Q

Caution giving norepinephrine to patients with ___.

A

hyperthyroidism, pheochromocytoma and without central IV access d/t extravasation

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23
Q

Class of Isoproterenol

A

Synthetic catecholamine, Non-selective beta-adrenergic agonist

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24
Q

Mechanism of Action of Isoproterenol

A

Agonizes beta receptors to acts on G proteins to ­increase cAMP, resulting in an influx of Ca++ causing clinical effects

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25
Q

Clinical Use of Isoproterenol & Route

A

β1 effects increase heart rate, contractility, and cardiac output.

β2 stimulation causes bronchodilation and a decrease in peripheral vascular resistance and diastolic blood pressure

Route: IV

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26
Q

Dosing of Isoproterenol

A

Infusion: 0.015–0.15 mcg/kg/min

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27
Q

Onset and DOA of Isoproterenol

A

Onset: 1 minute

DOA: 1 – 5 minutes

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28
Q

Metabolism and Excretion of Isoproterenol

A

Metabolism: COMT

Elimination: Renally excreted (50% unchanged)

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29
Q

Isoproterenol is a poor inotropic choice in most situations because ___.

A

myocardial oxygen demand increases while oxygen supply falls

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30
Q

Caution use of Isoproterenol in patients with what conditions?

A

CAD, hypertrophic cardiomyopathy, hyperthyroidism, pheochromocytoma

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31
Q

Class of Dopamine

A

endogenous nonselective adrenergic and dopaminergic agonist, direct and indirect acting

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32
Q

Mechanism of Action of Dopamine & Route

A

dopamine stimulates D receptors, β-receptors, and α-receptors in a dose-dependent manner because of differing receptor affinities.

Route: IV

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33
Q

Renal Dosing of Dopamine

A

Not scientifically supported (urine output increases, but long-term morbidity and mortality do not improve)

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34
Q

Dosing of Dopamine

A

Dopaminergic receptors: 2 mcg/kg/min

β receptors: 2 to 5 mcg/kg/min

α receptors: greater than 10 mcg/kg/min

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35
Q

Onset and DOA of Dopamine

A

Onset: 2 – 4 minutes

DOA: 10 minutes

36
Q

Metabolism and Excretion of Dopamine

A

Metabolism

•MAO and COMT ►75% inactive and 25% NE

Elimination: Renally excreted

37
Q

Considerations for Dopamine

A

Dopamine also inhibits aldosterone, resulting in an increase in sodium excretion and urine output.

Caution in patients on MAOI and TCA, tachycardia, arrythmias

r/f extravasation

38
Q

Class and Mechanism of Action of Dobutamine

A

Class: Synthetic catecholamine, selective beta 1 adrenergic agonist

Mechanism of Action

  • synthetic analog of isoproterenol
  • Acts on B1, G proteins to increase ­cAMP, influx of Ca causing increasing contractility & CO
  • Some B2 (vasodilation, decreases SVR) & A1 (min);
39
Q

Clinical Use and Route of Dobutamine

A

Clinical Use: Cardiogenic and septic shock, treat mild CHF, cardiac stress tests

Route: IV

40
Q

Dosing of Dobutamine

A

Infusion: 2 to 20 mcg/kg/min

41
Q

Onset and DOA of Dobutamine

A

Onset: 1 minute

DOA: 10 minutes

42
Q

Metabolism & Excretion of Dobutamine

A

Metabolism: MAO, COMT

Elimination: Renally excreted

43
Q

Caution use of dobutamine in patients with what conditions?

A

tachycardia, CAD, hypertrophic cardiomyopathy

44
Q

Dobutamine can cause __

A

Decrease SVR, platelet inhibition

45
Q

Class and Clinical Use of Phenylephrine

A

Class: Alpha 1 adrenergic agonists

Clinical Use: Vasodilatory shock, hypotension (with a normal heart rate), s/p spinal anesthesia

46
Q

Mechanism of Action of Phenylephrine & Route

A

Agonizes A1 receptors, activates IP3 which increases intracellular Ca and increases BP

Route: IV, intranasal, ocular

47
Q

Dosing of Phenylephrine

A

Small boluses of 40-80 mcg

Infusion: 20 – 50 mcg/min

48
Q

Onset and DOA of Phenylephrine

A

Onset: 1 minutes

DOA: 15 – 20 minutes

49
Q

Metabolism and Excretion of Phenylephrine

A

Metabolism: MAO

Elimination: Renally excreted

50
Q

Considerations for Phenylephrine

A
  • Reflex bradycardia mediated by the vagus nerve can reduce cardiac output
  • Caution in patients with bradycardia, hyperthyroidism, pheochromocytoma
  • Phenylephrine must be diluted from a 1% solution (10 mg/1-mL ampule), usually to a 100 mcg/mL solution and titrated to effect
51
Q

When would you administer phenylephrine instead of ephedrine?

A

If they have a normal HR

(If they are hypotensive AND bradycardic, give ephedrine instead)

52
Q

Class, Clinical Use and Route of Vasopressin

A

Class: Exogenous antidiuretic peptide & vasopressor

Clinical Use

Septic shock, post–cardiopulmonary bypass shock state

ACE Inhibitor related hypotension

Route: IV

53
Q

Mechanism of Action of Vasopressin

A

Vasoconstrict: stim V1 receptors on vascular smooth muscle, glomerular mesangial cells, & vasa recta; ADH (activate V2 receptors)

54
Q

Dosing of Vasopressin

A

Bolus: 1 – 20 units

infusion: 0.01-0.04 units/min

55
Q

Onset and DOA of Vasopressin

A

Onset: 1 – 5 minutes

DOA: 10 – 30 minutes

56
Q

Metabolism and Excretion of Vasopressin

A

Metabolism: Tissue peptidase metabolism

Elimination: Renally excreted

57
Q

Complications of vasopressin include ___.

A

gastrointestinal ischemia, decreased cardiac output, skin or digital necrosis, and cardiac arrest (especially at doses greater than 0.04 units/min)

58
Q

Class, Clinical Use & Route of Milrinone

A

Class: Phosphodiesterase 3 Inhibitor

Clinical Use

Cardiogenic shock, right heart failure, dilates pulmonary artery

Inotropy in the setting of beta blockade

Route: IV

59
Q

Mechanism of Action of Milrinone

A

Inhibition of (PDE) III degrades cAMP which decreases hydrolysis of cAMP & cGMP in myocardium & vascular smooth muscle

Myocardium: ­increase cAMP whichincreases ­intracellular Ca & increases contractile activation

Vascular smooth muscle: ­increase cAMP works to cause vasodilation & decrease PVR

60
Q

Class, Clinical Use & Route of Ephedrine

A

Class: Synthetic noncatecholamine, indirect and direct acting

Clinical Use

Treat hypotension with bradycardia

Used w/ GA or SNS blockade to ­increase BP, brady after spinal,

Like epinephrine, but weaker action and lasts 10x longer

Route: IV, IM

61
Q

Dosing of Ephedrine

A

Small Bolus: 5 - 10 mg

62
Q

Onset and DOA of Ephedrine

A

Onset: 1 minute

DOA: 10 – 60 minutes

63
Q

Metabolism and Excretion of Ephedrine

A

Metabolism: Resistant to MAO since lacks catecholamine

Elimination: Renally excreted (40% unchanged)

64
Q

Considerations for Ephedrine use

A

Avoid in patients with CAD, tachycardia, hypertension and patients taking MAOIs, TCAs & cocaine

  • Caution in trauma because subsequent doses are increased to offset the development of tachyphylaxis, which is probably due to depletion of norepinephrine stores.
  • Ephedrine is available in 1-mL ampules containing 25 or 50 mg of the agent
65
Q

Class and Clinical Use of Clonidine

A

Class: Alpha 2 adrenergic agonist

Clinical Use

Sedation, antihypertensive, postoperative shivering, alcohol withdrawal symptoms, and the treatment of acute postoperative pain and some chronic pain syndromes

Peripheral anesthesia – prolongs the duration of a block

66
Q

Mechanism of Action of Clonidine

A

Selectively activates α2 – adrenergic receptors & thereby inhibits sympathetic outflow from medulla which causes decreases HR, contractility, & vasomotor tone

Analgesia: α2 adrenergic receptor in dorsal horn produces anti-nociceptive state by inhibiting release of sub P & nociceptive neuron firing produced by painful stimuli.

67
Q

Dosing of Clonidine

A

Intravenous: 1–3 mcg/kg

68
Q

Metabolism and Excretion of Clonidine

A

Metabolism: ~50% of drug is metabolized in liver

Elimination: Renally excreted (~ 50% unchanged)

69
Q

Consideration of Clonidine

A

Clonidine potentiates anesthetic effects of other volatile or injectable anesthetics

Continuing the medication throughout the perioperative period is essential to avoid rebound hypertension

70
Q

Class, Clinical Use and Route of Albuterol

A

Class: Selective B2 agonists

Clinical Use: Bronchodilation

Route: Inhalation

71
Q

Mechanism of Action of Albuterol

A

Acts directly on b2 receptors,which when coupled to G protein, activates adenylyl cyclase which­ increases cAMP & decreases Ca+, increases K+ conductance causing smooth muscle relaxation & bronchodilation

72
Q

Dosing of Albuterol

A

90 mcg per puff

73
Q

Onset and DOA of Albuterol

A

Onset: 5 minutes

DOA: 4 hours

74
Q

Metabolism and Excretion of Albuterol

A

Metabolism: MAO

Elimination: Renally excreted (30 % unchanged)

75
Q

Albuterol can cause ____.

A

Tremors, tachycardia, hypokalemia

76
Q

If spetic shock, treated with ___.

A

norepinephrine and vasopressin (due to the fact that you’re dealing with peripheral vasiodilation from sepsis)

  • Epinephrine is the third line

Dopamine is inferior due to causing more arythmias

No phenylephrine becuase it decreases CO from ans increase in SVR

77
Q

If cardiogenic shock, pt needs ____.

A

Inotropy

If they’re hypotensive, give epinephrine

If they have poor CO but they’re not hypotensive, give dobutamine or milrinone

78
Q

If hemorrhagic shock, treat with ___.

A

rescuscitation instead of vasopressors

79
Q

Describe what’s going on with aortic stenosis, what is the goal? What is the treatment?

A

Aortic stenosis = heart pushing against fixed defect

Goal is to lower the HR because need time for LV to fill and push out against stenotic valve

USE PHENYLEPHRINE, alpha 1 causes systemic vasoconstriction with reflex bradycardia

80
Q

Pharmacological treatment of tamponade

A

Keep HR fast with increased inotropy

Use epinephrine

81
Q

Treatment of pulmonary hypertension with systemic hypotension

A

Use vasopressin alone because it is the only vasopressor that doesn’t affect the pulmonary vascular resistance

82
Q

If hypotensive with arrythmias, give___.

A

Phenylephrine or vasopressin because they do not have beta agonism

*If the patient is hypotensive because of an arrythmia, think about cardioversion rather than vasopressors.

83
Q

Dose of Milrinone

A

Dosing (IV)

  • Loading dose: 50 mcg/kg over ten minutes
  • Infusion: 0.375–0.75 mcg/kg /min
84
Q

Onset and Elimination of Milrinone

A

Distribution

•Onset: 5 – 15 minutes

Elimination

•Renally excreted (80% unchanged)

85
Q

Caution use of Milrinone in patients with ____

A

hypotension, renal failure

•Side effects include arrythmias

Anesthesia-phar (18 decks)

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